Paragigantocellularis potentiation of perforant path input to the dentate gyrus is attenuated by local β adrenergic blockade but not by LTP saturation

Munro, Catherine Anne M. (1995) Paragigantocellularis potentiation of perforant path input to the dentate gyrus is attenuated by local β adrenergic blockade but not by LTP saturation. Masters thesis, Memorial University of Newfoundland.

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Abstract

In vitro work indicates that both frequency mediated potentiation (LTP) and norepinephrine mediated potentiation (NEP) in the dentate gyrus of the hippocampus are attenuated by NMDA receptor blockade and/or β-receptor blockade, suggesting both forms of potentiation converge on a single form of plasticity (Stanton, Mody, & Heinemann, 1989) . However, in vivo work by Frizzell and Harley (Frizzell & Harley, 1994) indicates that locus coeruleus activated NEP can be induced when LTP has been occluded by intradentate application of the NMDA receptor antagonist ketamine. This suggests that in vivo NEP is independent of the LTP plasticity mechanism. The present study further explores the LTP/NE relationship. -- Stimulation of the nucleus paragigantocellularis (PGi) with a 333 Hz train 30 ms prior to single pulse stimulation of the perforant path (PP) input to the hippocampus results in presumed adrenergic mediated short-term potentiation of PP-evoked potentials recorded in the dentate gyrus which is occluded by a systemic β-blocker (Babstock & Harley, 1992). This form of NEP was used in the present study. Using both timolol and saline filled recording pipettes placed in the dentate gyrus, it was demonstrated that PGi stimulation is an effective method of producing NEP, that PGi-induced potentiation is locally mediated by β-receptors in the dentate gyrus and that LTP can be produced in the presence of intradentate application of β-blockers. Further, local β-blockade marginally reduces LTP induction but β-blockade has no effect on final LTP magnitude. An apparently independent PGi-induced potentiation persists following LTP saturation and following LTP saturation, PGi-induced potentiation can again be shown to be β-receptor dependent. These results support the hypothesis that there are two distinct, independent forms of plasticity which can be initiated in the dentate gyrus, β-mediated and NMDA mediated. Further, the changes induced by NE and high frequency stimulation appear to be additive.

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